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The pharmacology of antidepressants is not entirely clear.. The earliest and probably most widely accepted scientific theory of antidepressant action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the monoamine neurotransmitters (namely serotonin, norepinephrine and dopamine). [1]
Older and less selective antidepressants like TCAs and MAOIs inhibit the reuptake or metabolism of norepinephrine and serotonin in the brain, which results in higher concentrations of neurotransmitters. [25] Antidepressants that have dual mechanisms of action inhibit the reuptake of both serotonin and norepinephrine and, in some cases, inhibit ...
Another common type of antidepressant, SNRIs work in a similar way to SSRIs by increasing both serotonin and another neurotransmitter called norepinephrine. Common SNRIs include venlafaxine (sold ...
[192] [193] A large cohort study conducted by researchers in the Netherlands investigated the association between depressive disorders, symptoms, and antidepressants with inflammation. The study showed decreased levels of interleukin (IL)-6 , a cytokine that has proinflammatory effects, in patients taking SSRIs compared to non-medicated patients.
Some antidepressants are used as a treatment for social anxiety disorder, but their efficacy is not entirely convincing, as only a small proportion of antidepressants showed some effectiveness for this condition. Paroxetine was the first drug to be FDA-approved for this disorder.
Certain antidepressants are prescribed to treat anxiety because they target the neurotransmitters responsible for the feelings and symptoms that characterize anxiety disorders. Most ...
Escitalopram, a less recognizable term, is the generic name for this common prescription antidepressant. ... anxiety disorder of some kind. ... it referred to as the “feel good” neurotransmitter.
This delay can explain the reason why antidepressants do not have effect on depression immediately. This can also be the reason why the antidepressant mechanisms can be connected to the increasing neuro impulse flow from 5-HT neurons, where as the concentration of 5-HT increases at the axon terminal before SSRIs start to work properly.
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